Hashimoto’s Thyroiditis, named for Dr. Hakaru Hashimoto, who first identified it in 1912, is also called Hashimoto’s disease, and chronic lymphocytic thyroiditis. Hashimoto’s thyroiditis is an autoimmune disease in which the body’s own immune system attacks the thyroid gland. The thyroid is a small butterfly shaped endocrine gland in the front of the neck which makes hormones T3 (triiodothyronine), and T4 (thyroxine). These hormones regulate metabolism. The thyroid is controlled by hormones secreted by the pituitary gland.
The pituitary gland is a pea-sized gland located in the base of the brain which, among others, makes thyroid stimulating hormone, or TSH. TSH stimulates the thyroid to make thyroid hormone. In the case of Hashimoto’s thyroiditis, the thyroid cells are damaged, potentially resulting in the inability to make enough thyroid hormones to regulate metabolism properly. This is referred to as hypothyroidism. Hypothyroidism can cause body functions to become bradykinetic, including: heart rate, brain function, and ability to metabolize food for energy. Hashimoto’s disease is the commonest form of hypothyroidism.
People who get Hashimoto’s disease often have family members who have thyroid or other autoimmune diseases. People who get Hashimoto’s disease sometimes have other autoimmune diseases (Women’s Health, 2012). The causes of Hashimoto’s thyroiditis are not clearly understood. However, certain people are more likely than others to have this condition. In an article in Everyday Health, Lynn Marks stated the following factors that may increase one’s risk for developing the disease: Gender: Women are seven times more likely than men to develop Hashimoto’s thyroiditis. Age: The disease is diagnosed most often in middle-aged adults.
Other autoimmune diseases: Having other autoimmune diseases-such as rheumatoid arthritis, diabetes mellitus, or lupus increases your risk of getting Hashimoto’s thyroiditis. Genetics: You have a higher risk of developing the condition if other members of your family have thyroid or autoimmune diseases (Marks, n. d. ). Rheumatoid arthritis is a chronic disorder of the joints and cartilage, as well as some organs and body systems. Diabetes mellitus is an autoimmune insulin deficiency disorder caused by the destruction of certain cells in the pancreas that produce insulin characterized by hyperglycemia.
Lupus pertains to a group of skin or generalized collagen disorders, sometimes causing arthralgia, arthritis, leukopenia, or anemia, among others. Signs and symptoms of Hashimoto’s thyroiditis are sometimes ambiguous and similar to other conditions. The American Thyroid Association (n. d. ) asserted that many signs of Hashimoto’s are similar to other diseases or conditions. Because the condition usually progresses very slowly over many years, people with Hashimoto’s thyroiditis may not have any symptoms early on, even when the characteristic TPO (thyroid peroxidase) antibodies may be detected in blood tests.
TPO is an enzyme that plays a role in the production of thyroid hormones. However, over time, thyroiditis causes slow and chronic cell damage leading to the development of a goiter (thyromegaly) with gradual thyroid failure, and most patients will eventually develop symptoms of hypothyroidism. Hypothyroid symptoms may include fatigue, weight gain, constipation, increased sensitivity to cold, dry skin, depression, muscle aches and reduced exercise tolerance, and irregular or heavy menses (American Thyroid Association, n. d. ).
In order to diagnose Hashimoto’s thyroiditis, certain information must be ascertained. According to The National Institute of Diabetes and Digestive and Kidney Diseases, A diagnosis of Hashimoto’s thyroiditis begins with a physical exam and medical history. A goiter, nodules, or growths may be found during a physical exam, and symptoms may suggest hypothyroidism. Diagnostic blood tests may include the TSH, which, if above normal lab values, means a patient has hypothyroidism. Blood tests also include T4, which is the amount of thyroid hormone in the blood.
In hypothyroidism, the blood lab values are lower than normal. The anti-thyroid antibody tests look for presence of thyroid autoantibodies. Most people with Hashimoto’s disease have these antibodies; however, hypothyroidism isn’t always caused by Hashimoto’s disease. Other useful tools for diagnoses include: ultrasonography, or computerized tomography (CT) scan. These tools create images of the thyroid which can be studied and interpreted by a radiologist. Size and texture, as well as a pattern typical of inflammation are noted (NIDDK, 2014).
Treating patients diagnosed with Hashimoto’s thyroiditis is relatively straight forward. Patients with overt hypothyroidism (elevated TSH and low thyroid hormone levels), treatment consists of thyroid hormone replacement) (The American Thyroid Association, n. d. ). Synthetic levothyroxine is inexpensive and very effective in restoring normal thyroid hormone levels, and results in improvement of symptoms of hypothyroidism. Most patients with Hashimoto’s thyroiditis will require lifelong treatment with levothyroxine. When levothyroxine is taken in the appropriate dose, it has no side effects.
However, when an insufficient dose is taken, serum TSH remains elevated and patients may have persistent symptoms of hypothyroidism. If the dose is excessive, serum TSH will become suppressed and patients may develop symptoms of hyperthyroidism (American Thyroid Association n. d. ). In addition, a study found on selenium and autoimmune thyroiditis in Medscape revealed, Patients presenting with Hashimoto’s thyroiditis with normal T4 levels and normal or slightly elevated TSH levels because of the absence of levothyroxine therapy demonstrated a significant decrease in anti-TPO antibody levels following 12 months upplementation with sodium selenite administered at physiological doses.
Furthermore, on discontinuation of selenium supplementation, one study found that antibody levels increased to their initial levels after 3-6 months, while another study found that the antibody levels remained stable. In three studies, supplemented patients reported improved wellbeing, independently of the effect on anti-TPO antibodies. The positive effect appears to be related to a direct effect of selenium on cerebral and cognitive functions.
Safety was found to be excellent in most patients except in a few rare cases where gastrointestinal disorders were reported. (Drutel, A. , Archambeaud, F. , Caron, P. , 2013). Hashimoto’s disease may progress, and symptoms of an underactive thyroid can get worse without treatment. An untreated underactive thyroid can cause further problems, including: Infertility, miscarriage, giving birth to a baby with birth defects, and high cholesterol (hyperlipidemia. ) Severe underactive thyroid called myxedema can very rarely lead to: heart (cardiac) failure, seizures, coma, and death (Women’s Health, 2012).
Because women are most often affected by Hashimoto’s disease, care is needed before, after, and during pregnancy. Normal hormone changes during pregnancy cause thyroid hormone levels to increase. The thyroid may enlarge slightly in healthy women during pregnancy, but not enough to be felt. These changes do not affect the pregnancy or unborn baby. Yet, untreated thyroid problems can threaten pregnancy and the growing baby. Symptoms of normal pregnancy, like fatigue, can make it easy to overlook thyroid problems in pregnancy (Women’s Health, 2012).
Thyroid hormone is vital during pregnancy. The unborn baby’s brain and nervous system need thyroid hormone to develop. During the first trimester, the baby depends on the mother’s supply of thyroid hormone. At 10 to 12 weeks of pregnancy, the baby’s thyroid begins to work on its own (Women’s Health, 2012). Some women develop thyroid problems in the first year after giving birth. This is called postpartum thyroiditis. It often begins with symptoms of an overactive thyroid, which last 2 to 4 months. Mild symptoms might be overlooked.
Most women then develop symptoms of an underactive thyroid, which can last up to a year. An underactive thyroid needs to be treated. In most cases, thyroid function returns to normal as the thyroid heals (Women’s Health, 2012). There were two relevant findings when researching this topic. The first was found in The American Thyroid Association (n. d. ). This association stated that patients with elevated antibodies but normal thyroid function tests (TSH and Free thyroxine) do not require treatment.
If the Hashimoto’s patient has elevated TSH, they are then treated with synthetic thyroid hormone, known as levothyroxine to restore TSH levels to a normal range. Secondly, an article in Medscape revealed, Patients presenting with Hashimoto’s thyroiditis with normal T4 levels and normal or slightly elevated TSH levels because of the absence of levothyroxine therapy demonstrated a significant decrease in anti-TPO antibody levels following 12 months supplementation with sodium selenite administered at physiological doses.
Furthermore, on discontinuation of selenium supplementation, one study found that antibody levels increased to their initial levels after 3-6 months, while another study found that the antibody levels remained stable. In three studies, supplemented patients reported improved well-being, independently of the effect on anti-TPO antibodies. The positive effect appears to be related to a direct effect of selenium on cerebral and cognitive functions. Safety was found to be excellent in most patients except in a few rare cases where gastrointestinal disorders were reported (Drutel, A. Archambeaud, F. , Caron, P. , 2013).
Hashimoto’s thyroiditis is relatively common, particularly in women. Because of this, simple blood testing for antibodies and thyroid hormone levels should be a part of a yearly physical. Many health issues can be treated more effectively if found early, as in the case of thyroid disease. There are many ramifications if Hashimoto’s is left untreated. Fortunately, this condition is easily detected, and easily and inexpensively treated.
Congruently, anyone with other autoimmune conditions should be tested and treated if needed, conceivably making a more positive impact in dealing with those diseases. I have a family history of Hashimoto’s disease. I was diagnosed because my blood tests revealed thyroid antibodies; however my TSH is within normal ranges. I have blood testing done yearly to track the progress of the disease. Now that I have reached middle age, the possibility of having to take thyroid hormones increases.
I was aware of most of the information found in my research; however I wanted to find out if there were any new discoveries regarding Hashimoto’s disease. In fact, the study on selenium and the thyroid was intriguing. I am due for my annual check-up, and will take the newly found material on this topic to my endocrinologist to discuss the information. Overall, keeping up with information regarding one’s health issues is important. Finding new information could be potentially helpful, and could possibly preserve my own health and wellbeing, as well as helping to educate others with similar conditions.
